Atrial fibrillation is the most prevalent clinically relevant arrhythmia; a major cause of morbidity and hospitalization. Additionally, atrial fibrillation carries a significant risk of thrombo-embolic events, specifically cerebrovascular accident. Among the most prevalent risk factors for atrial fibrillation, hypertension not only has the strongest correlation but is also the most prevalent. The renin-angiotensin-aldosterone system represents a prime target for the treatment of hypertension through the use of angiotensin-converting enzymes inhibitors and angiotensin II receptor blockers. In addition to blood pressure control, these medications have been shown to reduce the occurrence of atrial fibrillation. They have been shown to have effects at the cellular level in preventing atrial fibrosis. Additionally, these medications may prevent the development ofatrial fibrillation, reduce the duration of atrial fibrillation, and facilitate electrical cardioversion in patients with the arrhythmia. Therefore, patients with, or at risk for atrial fibrillation may benefit from treatment with renin-angiotensin-aldosterone system antagonists; deriving benefits from these medications beyond simple blood pressure control.

• MeSH
• antagonisté receptorů pro angiotenzin terapeutické užití   MeSH
• fibrilace síní farmakoterapie   patofyziologie   MeSH
• inhibitory ACE terapeutické užití   MeSH
• lidé MeSH
• renin-angiotensin systém fyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• antagonisté receptorů pro angiotenzin MeSH
• inhibitory ACE MeSH

AIMS: Angiotensin converting enzyme inhibitors (ACEI) have been recently discussed in connection with the medical treatment of chronic subdural haematoma (CSDH). They may improve the treatment results. The objective of our study was to evaluate the impact of ACEI on the development of CSDH. The first question was to assess the impact of ACEI on postoperative CSDH healing. The second was to assess the impact of ACEI on the development of CSDH as such. PATIENTS AND METHODS: The study recruited patients treated surgically for CSDH at our department in the 2013-2018 period. Based on medical records, we retrospectively evaluated the clinical condition of the patients, their history (mainly pharmacological - the use of ACEI) and the course of treatment focussing on the reoccurrence of disease necessitating further therapeutic interventions. For the purpose of evaluating the impact of ACEI on postoperative CSDH healing, the patients were divided into two groups: those using ACEI and those without this medication. The results were compared. We also compared the prevalence of ACEI use in patients with CSDH with the prevalence of ACEI in the comparable population. The difference of the rates allowed us to evaluate the impact of ACEI on the development of CSDH itself. RESULTS: Of the 217 patients after surgery for CSDH, 79 continued the use of ACEI; the remaining 138 patients did not use this medication. Patients using ACEI after the surgery experienced a recurrence in 24 (30.4%) cases; patients without ACEI in 37 (26.8%) cases. A negligibly higher number of recurrences was recorded in patients with postoperative use of ACEI, but this difference was not statistically significant (P=0.574). Of a total of 230 patients who underwent surgery for CSDH, 81 were using ACEI chronically (35.2%). In the control group of 100 patients, 38 (38.0%) patients used ACEI. The difference was not statistically significant (P=0.629), so it is not possible to assume that ACEIs influence the development of CSDH as such. CONCLUSION: The initial high hopes for a positive ACEI effect on the healing of CSDH are now waived after the publication of several recent studies. According to our present knowledge, the development of CSDH does not appear to be influenced by ACEI use.

• Klíčová slova
• angiotensin converting enzyme inhibitors, burr hole drainage, chronic subdural haematoma, recurrence,
• MeSH
• chronický subdurální hematom * farmakoterapie   etiologie   MeSH
• drenáž MeSH
• inhibitory ACE škodlivé účinky   MeSH
• lidé MeSH
• recidiva MeSH
• retrospektivní studie MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• inhibitory ACE MeSH

The role of the intrarenal renin-angiotensin system (RAS) in the pathophysiology of malignant hypertension is not fully understood. Accumulating evidence indicates that the recently discovered vasodilator axis of the RAS, angiotensin-converting enzyme (ACE) type 2 (ACE2)/angiotensin 1-7 (ANG 1-7), constitutes an endogenous system counterbalancing the hypertensiogenic axis, ACE/angiotensin II (ANG II)/AT1 receptor. This study aimed to evaluate the role of the intrarenal vasodilator RAS axis in the pathophysiology of ANG II-dependent malignant hypertension in Cyp1a1-Ren-2 transgenic rats. ANG II-dependent malignant hypertension was induced by 13 days' dietary administration of indole-3-carbinol (I3C), a natural xenobiotic that activates the mouse renin gene in Cyp1a1-Ren-2 transgenic rats. It was hypothesized that pharmacologically-induced inhibition of the ACE2/ANG 1-7 complex should aggravate, and activation of this axis should attenuate, the course of ANG II-dependent malignant hypertension. Blood pressure (BP) was monitored by radiotelemetry. ACE2 inhibitor (DX 600, 0.2 μg/day) and ACE2 activator (DIZE, 1 mg/day) were administrated via osmotic minipumps. Even though ACE2 inhibitor significantly decreased and ACE2 activator increased intrarenal ANG 1-7 concentrations, the course of BP, as well as of albuminuria, cardiac hypertrophy and renal glomerular damage, were not altered. It was shown that intrarenal alterations in the ACE2/ANG 1-7 complex did not significantly modify the course of malignant hypertension in I3C-induced Cyp1a1-Ren-2 transgenic rats. Thus, in our experimental setting alterations of this intrarenal vasodilator complex of the RAS do not significantly modify the form of malignant hypertension that clearly depends on the inappropriately increased activity of the ACE/ANG II/AT1 receptor axis.

• Klíčová slova
• angiotensin 1-7, angiotensin II, angiotensin-converting enzyme type 2, malignant hypertension, renin-angiotensin system,
• MeSH
• aktivátory enzymů farmakologie   MeSH
• albuminurie komplikace   MeSH
• angiotensin I metabolismus   MeSH
• angiotensin konvertující enzym metabolismus   MeSH
• angiotensin-konvertující enzym 2 MeSH
• cytochrom P-450 CYP1A1 genetika   MeSH
• diminazen analogy a deriváty   farmakologie   MeSH
• hypertenze maligní komplikace   metabolismus   patofyziologie   moč   MeSH
• krevní tlak účinky léků   MeSH
• krysa rodu Rattus MeSH
• ledviny účinky léků   metabolismus   MeSH
• myši MeSH
• peptidové fragmenty metabolismus   MeSH
• peptidy farmakologie   MeSH
• potkani transgenní MeSH
• regulace genové exprese účinky léků   MeSH
• renin-angiotensin systém účinky léků   MeSH
• renin genetika   MeSH
• sodík moč   MeSH
• tělesná hmotnost účinky léků   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Ace2 protein, mouse MeSH Prohlížeč
• Ace2 protein, rat MeSH Prohlížeč
• aktivátory enzymů MeSH
• angiotensin I (1-7) MeSH Prohlížeč
• angiotensin I MeSH
• angiotensin konvertující enzym MeSH
• angiotensin-konvertující enzym 2 MeSH
• cytochrom P-450 CYP1A1 MeSH
• diminazen MeSH
• diminazene aceturate MeSH Prohlížeč
• DX600 peptide MeSH Prohlížeč
• peptidové fragmenty MeSH
• peptidy MeSH
• Ren2 protein, mouse MeSH Prohlížeč
• renin MeSH
• sodík MeSH

The angiotensin converting enzyme (ACE) gene is located on human chromosome 17 expressing three genotypes within the intron 16 of the related gene structure. These genotypes are classified as I and D alleles which are termed as insertion and deletion, respectively. This study was carried out to identify possible relationships between the insertion/deletion (I/D) polymorphisms and athletic performance in Turkish athletes. To be able to determine these relationships, eighty healthy athletes and eighty healthy sedentary controls were genotyped for the ACE I/D polymorphism at gene level. According to the results obtained, we found significant difference on ACE I/D polymorphism in between athletes and healthy controls (x2 = 7.32, df = 2, P = 0.026). This result supports the association in ACE genotype in Turkish athletes, suggesting that this might be a genetic factor influencing the physical performance.

• MeSH
• angiotensin konvertující enzym genetika   MeSH
• dospělí MeSH
• fyzická vytrvalost MeSH
• genotyp MeSH
• lidé MeSH
• polymorfismus genetický * MeSH
• sporty * MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Turecko MeSH
• Názvy látek
• angiotensin konvertující enzym MeSH

To prove whether the interaction between insertion/deletion (I/D) angiotensin I converting enzyme (ACE) and M235T angiotensinogen (AGT) gene polymorphic alleles could contribute to causing essential hypertension, we examined subjects from the Czech Republic (365 Caucasians total; 202 normotensives and 163 hypertensives). Subjects were genotyped for insertion/deletion polymorphism of ACE (I/D ACE, intron 16) and for M235T polymorphism of angiotensinogen gene (AGT, exon 2) by means of the polymerase chain reaction (PCR) method. The case-control approach was used. Fisher's exact test followed by Holmes's test to overcome the problem of multiple comparisons were used for the statistical analysis of data. No association of single gene allelic variants with essential hypertension was found in our population. Having compared only double homozygote combinations, the association of the DDMM genotype with essential hypertension was proven (P = 0.0081). To the contrary, IITT (P = 0.0086) was found more frequently in normotensive subjects. We conclude that the interaction of the I/D ACE and M235T AGT polymorphic alleles can contribute to essential hypertension, despite the absence of single gene associations with the condition.

• MeSH
• alely MeSH
• angiotensin konvertující enzym genetika   MeSH
• angiotensinogen genetika   MeSH
• dospělí MeSH
• genetická variace MeSH
• genotyp MeSH
• geny fyziologie   MeSH
• homozygot MeSH
• hypertenze genetika   MeSH
• index tělesné hmotnosti MeSH
• lidé středního věku MeSH
• lidé MeSH
• polymorfismus genetický genetika   MeSH
• pravděpodobnost MeSH
• předpověď MeSH
• referenční hodnoty MeSH
• studie případů a kontrol MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• angiotensin konvertující enzym MeSH
• angiotensinogen MeSH

Heart failure has become the most widely studied syndrome in cardiology over the recent years. Despite the encouraging achievements by angiotensin converting enzyme (ACE) inhibitors, the mortality of patients with chronic heart failure remains high. There are several factors which can potentially be responsible for the fact that about 80% of patients with a failing heart defy protection by ACE inhibitors: different activation of tissue and systemic renin-angiotensin system (RAS) in a particular heart disease and the distinct ability of various ACE inhibitors to block cardiac ACE, alternative pathways for angiotensin II formation (chymase), genetic polymorphism of the RAS system and the complexity of neuroendocrine activation. Moreover, chronic heart failure can provoke disturbances in the reactivity of peripheral vessels and metabolism of striated muscles. These factors may then potentiate the vicious circle of heart failure. New therapeutic approaches, which could further reduce the mortality in patients with heart failure involve angiotensin II type 1 receptor antagonists, beta-blockers, aldosterone antagonists and blockers of the endothelin receptor. A number of questions associated with functions of the RAS still remain open and their solution could be of substantial benefit for patients with a failing heart.

• MeSH
• antagonisté endotelinového receptoru MeSH
• antagonisté mineralokortikoidních receptorů terapeutické užití   MeSH
• antagonisté receptorů pro angiotenzin MeSH
• beta blokátory terapeutické užití   MeSH
• inhibitory ACE terapeutické užití   MeSH
• lidé MeSH
• nízký srdeční výdej farmakoterapie   mortalita   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antagonisté endotelinového receptoru MeSH
• antagonisté mineralokortikoidních receptorů MeSH
• antagonisté receptorů pro angiotenzin MeSH
• beta blokátory MeSH
• inhibitory ACE MeSH

There is little data regarding the impact of renin-angiotensin system (RAS) gene polymorphisms on tuberculosis. The current study designed to survey the possible association between RAS polymorphisms and the risk of pulmonary tuberculosis (PTB) in a sample of the southeast Iranian population. This case-control study was done on 170 PTB patients and 170 healthy subjects. The AGT rs699 C>T, ACE rs4341 C>G and AT1R rs5186 C>A variants were genotyped using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) and ACE rs4646994 (287bp I/D) variant by PCR method. Regarding AT1R rs5186 A>C polymorphism, the findings revealed that AC genotype and C allele significantly decreased the risk of PTB (OR=0.39, 95% CI=0.22-0.67, p=0.001, and OR=0.53, 95% CI=0.25-0.72, p=0.002, C vs. A, respectively). The TC genotype and C allele of AGT rs699 T>C significantly associated with decreased the risk of PTB (OR=0.45, 95% CI=0.28-0.74, p=0.002, TC vs. TT and OR=0.51, 95% CI=0.32-0.80, p=0.005, C vs. T, respectively). The ID genotype of ACE 287bp I/D significantly increased the risk of PTB (OR=1.88, 95% CI=1.12-3.17, p=0.017). Our finding did not support an association between ACE rs4341 C>G variant and the risk of PTB. In summary, the findings revealed an association between AT1R rs5186 A>C, AGT rs699 T>C and ACE 287bp I/D polymorphisms and the risk of PTB in a sample of the southeast Iranian population. Further investigation with higher sample sizes and diverse ethnicities are required to confirm our findings.

• Klíčová slova
• Angiotensin, Angiotensin converting enzyme, Angiotensin type 1 receptor, Polymorphism, Tuberculosis,
• MeSH
• angiotensin konvertující enzym * genetika   MeSH
• angiotensinogen genetika   MeSH
• genetická predispozice k nemoci MeSH
• genotyp MeSH
• lidé MeSH
• plicní tuberkulóza * genetika   MeSH
• polymorfismus genetický MeSH
• receptor angiotensinu typ 1 genetika   MeSH
• studie případů a kontrol MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Írán epidemiologie   MeSH
• Názvy látek
• ACE protein, human MeSH Prohlížeč
• AGT protein, human MeSH Prohlížeč
• AGTR1 protein, human MeSH Prohlížeč
• angiotensin konvertující enzym * MeSH
• angiotensinogen MeSH
• receptor angiotensinu typ 1 MeSH

Angiotensin converting enzyme (ACE) is a zinc metallopeptidase which plays a key role in the regulation of important vasoactive peptides through its proteolytic activity. Effective inhibitors of ACE were until recently designed in the absence of the solved 3D structure of this enzyme. About 15 ACE inhibitors are currently commercially available, all of which nonspecifically inhibit both active domains of ACE. Vasopeptidase inhibitors are mixed inhibitors of ACE and neutral endopeptidase (NEP). They contemporarily inhibit the catalytic function of two enzymes and currently are undergoing clinical trials exhibiting better efficacy in the treatment of hypertension and cardiovascular diseases, but in the same time higher risk of adverse side effects compared to ACE inhibitors.

• MeSH
• inhibitory ACE * chemie   farmakologie   MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• inhibitory ACE * MeSH

Angiotensin I converting enzyme (ACE) participates not only in the regulation of the extracellular fluid volume and blood pressure but also in the control of proliferating processes in the human organism. The favourable effect of ACE inhibitors in the treatment of essential hypertension may be caused also by their antiproliferative effect. The development of essential hypertension is probably of polygenic origin. The gene for ACE, and its alleles encountered commonly in the population is involved in the pathophysiology of systemic hypertension by acting on the dynamic properties of processes in the organism which regulate changes of the extracellular fluid volume and proliferation. Therefore it is necessary, when treating systemic hypertension with ACE inhibitors, to pay attention to monitoring of the blood pressure and organ changes. The relationship with blood pressure assessed by conventional methods need not be close. The antiproliferative effect of ACE inhibitors may be favourable in the treatment of hypertension and its clinical use in oncology may be taken into consideration.

• MeSH
• hypertenze farmakoterapie   patofyziologie   MeSH
• inhibitory ACE farmakologie   terapeutické užití   MeSH
• krevní tlak účinky léků   MeSH
• lidé MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• Názvy látek
• inhibitory ACE MeSH

BACKGROUND: Recurrent aphthous stomatitis (RAS) is multifactorial disease with unclear etiopathogenesis. The aim of this study was to determine distribution of the angiotensin I converting enzyme (ACE) gene polymorphisms and their influence on RAS susceptibility in Czech population. METHODS: The study included 230 subjects (143 healthy controls and 87 patients with RAS) with anamnestic, clinical and laboratory data. Five ACE gene polymorphisms (rs4291/rs4305/rs4311/rs4331/rs1799752 = ACE I/D) were determined by TaqMan technique. RESULTS: The allele and genotype distributions of the studied ACE I/D polymorphisms were not significantly different between subjects with/without RAS (Pcorr > 0.05). However, carriers of II genotype were less frequent in the RAS group (OR = 0.48, 95% CI = 0.21-1.12, P = 0.059). Stratified analysis by sex demonstrated lower frequency of II genotype in women (OR = 0.33, 95% CI = 0.09-1.17, P < 0.035, Pcorr > 0.05, respectively) than in men with RAS (P > 0.05). Moreover, the frequency of AGTGD haplotype was significantly increased in RAS patients (OR = 13.74, 95% CI = 1.70-110.79, P = 0.0012, Pcorr < 0.05). In subanalysis, TGD haplotype was significantly more frequent in RAS patients (P < 0.00001) and CGI haplotype was less frequent in RAS patients (P < 0.01), especially in women (P = 0.016, Pcorr > 0.05). CONCLUSIONS: Our study indicates that while the AGTGD and TGD haplotypes are associated with increased risk of RAS development, CGI haplotype might be one of protective factors against RAS susceptibility in Czech population.

• Klíčová slova
• Angiotensin I converting enzyme, Haplotype, Polymorphism, Recurrent aphthous stomatitis, Sex difference,
• MeSH
• aftózní stomatitida * epidemiologie   genetika   MeSH
• angiotensin konvertující enzym * genetika   MeSH
• frekvence genu MeSH
• genetická predispozice k nemoci MeSH
• lidé MeSH
• polymorfismus genetický MeSH
• studie případů a kontrol MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH
• Názvy látek
• ACE protein, human MeSH Prohlížeč
• angiotensin konvertující enzym * MeSH